The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P < 0.001); however, the magnitude of reduction did not differ between groups (P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal PCO(2) were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.
Nonvented "aerodynamic helmets" reduce wind resistance but may increase head (Th) and gastrointestinal (Tgi) temperature and reduce performance when worn in hot conditions. This study tested the hypothesis that Th and Tgi would be greater during low-intensity cycling (LIC) in the heat while wearing an aero helmet (AERO) vs. a traditional vented racing helmet (REG). This study also tested the hypothesis that Th, Tgi, and finish time would be greater, and power output would be reduced during a self-paced time trial in the heat with AERO vs. REG. Ten highly trained heat-acclimated endurance athletes conducted LIC (50% V[Combining Dot Above]O2max, LIC) and a high-intensity 12-km self-paced time trial (12-km TT) on a cycle ergometer in 39° C on 2 different days (AERO and REG), separated by >48 hours. During LIC, Th was higher at minute 7.5 and all time points thereafter in AERO vs. REG (p < 0.05). Similarly, during the 12-km TT, Th was higher at minutes 12.5, 15, and 17.5 in AERO vs. REG (p < 0.05). Heart rate (HR) and Tgi increased during LIC and during 12-km TT (both p < 0.001); however, no significant interaction (helmet × time) existed for HR or Tgi at either intensity (all p > 0.05). No group differences existed for finish time or power output during the 12-km TT (both p > 0.05). In conclusion, Th becomes elevated during cycling in the heat with an aero helmet compared with a traditional vented racing helmet during LIC and high-intensity cycling, yet Tgi and HR responses are similar irrespective of helmet type and Th. Furthermore, the higher Th that develops when an aero helmet is worn during cycling in the heat does not affect power output or cycling performance during short-duration high-intensity events.
The mechanism(s) responsible for heat stress induced reductions in orthostatic tolerance are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. Thus, heat stress mediated reductions in cerebral perfusion may explain the variation in tolerance in this thermal condition. This study tested the hypothesis that individuals with the greatest heat‐stress induced reduction in orthostatic tolerance would have the largest reduction in cerebral perfusion in this thermal condition. On different days, lower body negative pressure (LBNP) was imposed on 15 individuals during normothermia, and after a 1.5 °C rise in core temperatures (Tc). Tolerance was quantified as cumulative stress index (CSI) and the difference in CSI (CSIdiff) between thermal conditions was used to categorize individuals most (HighDif) and least (LowDif) affected. Heat stress reduced cerebral vascular conductance (CVC) relative to normothermia in both groups (P<0.05 for each); however, the magnitude of reduction in CVC was similar between groups (HighDif: 31.3±24.9 cm·s−1·mmHg−1; LowDif: 11.4±19.2 cm·s−1·mmHg−1, P=0.18). Our data indicate that variability in heat stress induced reductions in orthostatic tolerance is not related to reductions in cerebral perfusion in this thermal condition.
An increase in internal temperature renders individuals more susceptible to syncope during a simulated hemorrhage challenge relative to during normothermia but the extent of this susceptibility varies amongst individuals. The objective of this study was to investigate the role of plasma angiotensin II (AngII) in this interindividual variability. This study tested the hypothesis that individuals with the greatest reduction in orthostatic tolerance between normothermic and heat stress conditions would have the smallest heat‐stress induced increase in plasma AngII. On separate days, 10 individuals were subjected to a maximal simulated hemorrhage challenge via a lower body negative pressure (LBNP) protocol. One trial was conducted under normothermic conditions and the other under hyperthermic conditions, following a 1.5 °C increase in internal temperature. Tolerance was quantified as cumulative stress index (CSI); calculated by summing the product of the LBNP and the time at each level until the test was terminated (i.e., 10 mmHg × 3 min + 20 mmHg × 3 min + 30 mmHg × 3 min, etc.). There was no correlation between the difference in CSI and the increase in plasma AngII from normothermic to heat‐stress conditions (r=0.05, p>.05). These results indicate that plasma AngII does not play a role in the interindividual variability in the tolerance to a simulated hemorrhage challenge during heat stress.
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